Neurotransmitters Flashcards

1
Q

What are the 5 criteria of a neurotransmitter

A
synthesis:
must be made in pre-synaptic neuronal 
storage:
presynaptically 
but not nitrous oxide 
release:
must be released on demand 
inactivation:
must be inactivated
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2
Q

Main classifications of NT

A

amino acids
biogenic amines
peptides

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3
Q

examples of amino acid NT

A

glutamate
GABA
Glycine

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4
Q

two classes of biogenic NT

A
catecholamines:
noradrenaline 
adrenaline 
dopamine 
indolamines:
serotonin
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5
Q

glutamate

A

primary excretory NT in the CNS
involved in memory, learning and cell death
postsynaptically via inonotropic receptors

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6
Q

GABA

A

inhibitory NT in the CNS

acts via chloride channels

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7
Q

Glycine

A

inhibitory NT in the CNS

but is primary in the spinal cord and brainstem

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8
Q

`What are the three types of glutamate receptors

A
NMDA 
-Calcium ions 
Kainate 
-sodium and potassium ions
AMPA 
-permeable to cations (calcium, sodium and potassium)
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9
Q

(dys)functions of glutamate

A
  • synaptic plasticity
    synapses are strengthened or weakened by feedback mechanisms
  • excitotoxicity
    excessive stimulation of NMDA receptors causes a large influx of calcium ions, can result in cell death
    -migraine
    Karl Lashleys visual aura, implicated in cortical spreading depression
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10
Q

tell me about the causes epilepsy

A

excess excitation causes a feedback loop
uncontrolled excitation over expanding areas in the brain
can begin as partial seizures, if they become more uncontrolled, can become gran Mal seizures

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11
Q

What can seizures be treated with

A

phenytoin
- increases the refractory period between firings in voltage gated sodium channels

benzodiazepines
increase the action go GABA (because its an inhibitory NT)

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12
Q

Benzodiazepines

A

act on a separate receptor binding site on the GABA receptor subtype than GABA..
This controls the a ability of GABA to open the channel as when its bound the channel can open more frequently.

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13
Q

GABA

A

Found predominantly in the interneurons of the CNS - modules depending motor information
Acts on ligand gated chloride channels
Inactivated by presynaptic reuptake

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14
Q

Tell me about alcoholism

A

causes a change in GABA transmission, withdrawal results in convulsive movements and seizures
Can be treated with benzodiazepines and phenytoin

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15
Q

Glycine

A

second most common inhibitory NT in the CNs

But has major effects in the spinal cord and brainstem

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16
Q

Tell me about tetanus

A

caused by toxin clostridium tetani
inhibits the release of glycine
-shifts excitation-inhibition balance
mild effects restricted to muscles innervated by cranial nerves
more serious effects include epileptiform fits
treated with anti-toxin and benzodiazepines

17
Q

dopamine

A

NT and neuromodulator

involved with pleasure , addition and movement

18
Q

noradrenaline

A

sympathetic fight or flight response NT

decrease potentially associated in Parkinson’s and ADHD

19
Q

Adrenaline

A

sympathetic
peripheral hormone from adrenal medulla
SYNTHESISED IN THE BOUTON AND INACTIVATED PRINCIPALLY BY RE-UPTAKE

20
Q

Effects of dopamine

A

parkinsons
tremor, muscle rigidity due to depleted dopamine in the motor coordination circuits
schizophrenia
over production of dopamine in the mesolimibic system
Addiction
works through pleasure centres of the CNS located in the mesolimbic dopamine system

21
Q

effects of serotonin

A

depression and OCD

can be treated with fluoxetine as this is a serotonin reuptake inhibitor

22
Q

effects of endorphins and encephalins

A

pain
act on opioid receptors and endogenous ligands , opioids cause the down regulation of opiod receptors in the CNS
leads to opioid tolerance and increased intake

emotional perception:
naloxone can reduce symptoms

23
Q

acetylcholine - esters

A

found in both PNS and CNS (neuromuscular junction)
CNS:
-neurons project to the hippocampus and cortex
regions essential for the formation of new memories and learning

24
Q

Alzheimers disease

A

associated with dysfunction (reduction/) of ACh in the CNS

25
Q

Nicotine

A

acts on nicotinic acetylcholine receptors found in the PNS and the CNS

26
Q

Anticholinesterases

A

prevent breakdown of ACh therefore prolonging its activity

Can be therapeutic but also toxic